Affiliations: [a] Laboratoire Européen Performance Santé Altitude (LEPSA), EA 4604, Université de Perpignan Via Domitia, Font Romeu, France
| [b] Laboratoire Interuniversitaire de Biologie de la Motricité (LIBM) EA7424, Team laquo Vascular Biology and Red Blood Cell raquo, Université Claude Bernard Lyon 1, Université de Lyon, France
| [c] Laboratoire d’Excellence du Globule Rouge (Labex GR-Ex), PRES Sorbonne, Paris, France
| [d] Hospital Universitario German Trias i Pujol, Badalona, Spain
| [e] Unité de recherche Pluridisciplinaire Sport Santé Société (URePSSS), EA 7369, Université Lille, Université Artois, Université Littoral Côte d’Opale, Lille, France
Correspondence:
[*]
Corresponding author: Antoine Raberin, Laboratoire Européen Performance Santé Altitude (LEPSA), EA 4604, Université de Perpignan Via Domitia, Font Romeu, France. Tel.: +33 682 173 800; E-mail: antoine.raberin@gmail.com.
Note: [1] These author contributed equally to this work.
Abstract: Blood rheology and hemodynamic parameters have never been explored together during acclimatization to altitude. This study aimed to investigate changes in blood rheology parameters and pulmonary hemodynamics during the first days of real moderate altitude exposure. Seventeen athletes were tested at sea-level, 20 hours after their arrival at 2,400 meters of altitude (H1) and five days later (H2). Blood was sampled to analyze red blood cell (RBC) aggregation, blood viscosity and hematocrit. Pulmonary arterial pressure (PAP), pulmonary capillary pressure (Pcap) and pulmonary vascular resistance (PVR) were assessed by echocardiography. We observed a rise in hematocrit, blood viscosity, RBC aggregation, PAP, Pcap and PVR between sea-level and H1. In H2, RBC aggregation, hematocrit, PAP, Pcap and PVR remained different compared to sea-level and no difference was observed between H1 and H2. Blood viscosity decreased in H2 and returned to sea-level values. Our results suggest that hemoconcentration occurring within the first hours of altitude exposure increased blood viscosity, which contributed to the changes in pulmonary hemodynamic. When blood viscosity decreased in H2, no change occurred in pulmonary hemodynamic parameters suggesting that hypoxic pulmonary vasoconstriction was still present. The elevated RBC aggregation observed after in H2 could participate in the increase of Pcap.
